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Prostaglandin E2 inhibits and indomethacin enhances noradrenaline release in isolated kidneys of adult spontaneously hypertensive rats.前列腺素E2抑制而消炎痛增强成年自发性高血压大鼠离体肾脏中去甲肾上腺素的释放。
Br J Clin Pharmacol. 1990;30 Suppl 1(Suppl 1):165S-167S. doi: 10.1111/j.1365-2125.1990.tb05495.x.
2
Prostaglandin E2 inhibits noradrenaline release and purinergic pressor responses to renal nerve stimulation at 1 Hz in isolated kidneys of young spontaneously hypertensive rats.前列腺素E2可抑制年轻自发性高血压大鼠离体肾脏中去甲肾上腺素的释放以及对1赫兹肾神经刺激的嘌呤能升压反应。
J Hypertens. 1990 Oct;8(10):897-908. doi: 10.1097/00004872-199010000-00003.
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Effects of endogenous and synthetic prostanoids, the thromboxane A2 receptor agonist U-46619 and arachidonic acid on [3H]-noradrenaline release and vascular tone in rat isolated kidney.内源性和合成类前列腺素、血栓素A2受体激动剂U-46619及花生四烯酸对大鼠离体肾脏中[3H]-去甲肾上腺素释放及血管张力的影响
Br J Pharmacol. 1989 Jul;97(3):819-28. doi: 10.1111/j.1476-5381.1989.tb12021.x.
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Alpha 2D-adrenoceptors modulate renal noradrenaline release in normotensive and spontaneously hypertensive rats.α2D - 肾上腺素能受体调节正常血压和自发性高血压大鼠的肾去甲肾上腺素释放。
Eur J Pharmacol. 1994 Dec 27;271(2-3):283-92. doi: 10.1016/0014-2999(94)90785-4.
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Defective modulation of noradrenergic neurotransmission by endogenous prostaglandins in aging spontaneously hypertensive rats.内源性前列腺素对衰老自发性高血压大鼠去甲肾上腺素能神经传递的调节缺陷。
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Activation of beta 2-adrenoceptors by isoprenaline and adrenaline enhances noradrenaline release in cortical kidney slices of young spontaneously hypertensive rats.异丙肾上腺素和肾上腺素对β2 - 肾上腺素能受体的激活增强了年轻自发性高血压大鼠肾皮质切片中去甲肾上腺素的释放。
Naunyn Schmiedebergs Arch Pharmacol. 1992 Jan;345(1):25-32. doi: 10.1007/BF00175465.
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Role of prostanoids in the increased vascular responsiveness and delayed tachyphylaxis to serotonin in the kidney of spontaneously hypertensive rats.前列腺素类物质在自发性高血压大鼠肾脏中血管反应性增加及对血清素迟发性快速耐受中的作用。
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Role of prostaglandins in the increased vascular responsiveness to bradykinin in kidneys of spontaneously hypertensive rats.前列腺素在自发性高血压大鼠肾脏中血管对缓激肽反应性增强方面的作用。
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Evidence for enhanced inhibitory modulation by cyclooxygenase products of noradrenergic neurotransmission in the mesenteric vasculature of young spontaneously hypertensive rats.年轻自发性高血压大鼠肠系膜血管中去甲肾上腺素能神经传递的环氧化酶产物增强抑制性调节的证据。
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Alpha-adrenoceptor modulation of norepinephrine and ATP release in isolated kidneys of spontaneously hypertensive rats.自发性高血压大鼠离体肾脏中去甲肾上腺素和三磷酸腺苷释放的α-肾上腺素能受体调节
Hypertension. 1995 Jun;25(6):1224-31. doi: 10.1161/01.hyp.25.6.1224.

引用本文的文献

1
Activation of beta 2-adrenoceptors by isoprenaline and adrenaline enhances noradrenaline release in cortical kidney slices of young spontaneously hypertensive rats.异丙肾上腺素和肾上腺素对β2 - 肾上腺素能受体的激活增强了年轻自发性高血压大鼠肾皮质切片中去甲肾上腺素的释放。
Naunyn Schmiedebergs Arch Pharmacol. 1992 Jan;345(1):25-32. doi: 10.1007/BF00175465.

本文引用的文献

1
Renal sympathetic activity in spontaneously hypertensive rats and normotensive controls, as studied by three different methods.通过三种不同方法研究自发性高血压大鼠和正常血压对照大鼠的肾交感神经活动。
Acta Physiol Scand. 1984 Feb;120(2):265-72. doi: 10.1111/j.1748-1716.1984.tb00133.x.
2
Renal nerves in the pathogenesis of hypertension in experimental animals and humans.肾神经在实验动物和人类高血压发病机制中的作用
Am J Physiol. 1983 Jul;245(1):F1-14. doi: 10.1152/ajprenal.1983.245.1.F1.
3
Alterations in the release of norepinephrine at the vascular neuroeffector junction in hypertension.
Annu Rev Pharmacol Toxicol. 1985;25:621-41. doi: 10.1146/annurev.pa.25.040185.003201.
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Noradrenaline release and sympathetic nervous system activity.
J Hypertens. 1985 Apr;3(2):117-29. doi: 10.1097/00004872-198504000-00003.
5
Modulation of renal noradrenaline release by prejunctional receptor systems in vitro.体外研究节前受体系统对肾去甲肾上腺素释放的调节作用。
Clin Exp Pharmacol Physiol. 1987 May;14(5):423-8. doi: 10.1111/j.1440-1681.1987.tb00993.x.
6
Effects of endogenous and synthetic prostanoids, the thromboxane A2 receptor agonist U-46619 and arachidonic acid on [3H]-noradrenaline release and vascular tone in rat isolated kidney.内源性和合成类前列腺素、血栓素A2受体激动剂U-46619及花生四烯酸对大鼠离体肾脏中[3H]-去甲肾上腺素释放及血管张力的影响
Br J Pharmacol. 1989 Jul;97(3):819-28. doi: 10.1111/j.1476-5381.1989.tb12021.x.
7
Modulation of norepinephrine release through alpha 1- and alpha 2-adrenoceptors in rat isolated kidney.通过大鼠离体肾脏中的α1和α2肾上腺素能受体调节去甲肾上腺素释放
J Cardiovasc Pharmacol. 1987 Apr;9(4):500-7. doi: 10.1097/00005344-198704000-00016.
8
Regulation of noradrenaline release by presynaptic receptor systems.突触前受体系统对去甲肾上腺素释放的调节。
Rev Physiol Biochem Pharmacol. 1977;77:1-124. doi: 10.1007/BFb0050157.

前列腺素E2抑制而消炎痛增强成年自发性高血压大鼠离体肾脏中去甲肾上腺素的释放。

Prostaglandin E2 inhibits and indomethacin enhances noradrenaline release in isolated kidneys of adult spontaneously hypertensive rats.

作者信息

Rump L C, Wilde K, Schollmeyer P

机构信息

Department of Internal Medicine IV, University of Freiburg, FRG.

出版信息

Br J Clin Pharmacol. 1990;30 Suppl 1(Suppl 1):165S-167S. doi: 10.1111/j.1365-2125.1990.tb05495.x.

DOI:10.1111/j.1365-2125.1990.tb05495.x
PMID:2268506
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1368125/
Abstract

Renal neurotransmission and its modulation by prostaglandin (PG) E2 (0.06 microM) and indomethacin (10 microM) was investigated in isolated kidneys of adult spontaneously hypertensive (SHR) and normotensive control (WKY) rats. After preincubation with [3H]-noradrenaline the renal nerves were stimulated. The stimulation induced (S-I) outflow of radioactivity was taken as an index of noradrenaline release. The S-I outflow of radioactivity from SHR and WKY kidneys was similar but S-I pressor responses were enhanced in kidneys of SHR. PGE2 inhibited and indomethacin enhanced the S-I outflow of radioactivity in kidneys of WKY and SHR to a similar extent. This inhibitory effect of PGE2 is due to activation of inhibitory prejunctional PGE2 receptors. Neuronally released noradrenaline stimulates a local formation of PGE2 which then transjunctionally inhibits noradrenaline release. Renal noradrenaline release in the adult SHR and its modulation by PGs is not altered. An enhanced postjunctional responsiveness of the renal vasculature may contribute to the maintenance of hypertension in the adult SHR.

摘要

在成年自发性高血压（SHR）大鼠和正常血压对照（WKY）大鼠的离体肾脏中，研究了肾神经传递及其受前列腺素（PG）E2（0.06微摩尔）和吲哚美辛（10微摩尔）的调节情况。在用[3H] - 去甲肾上腺素预孵育后，刺激肾神经。将刺激诱导的（S - I）放射性流出作为去甲肾上腺素释放的指标。SHR和WKY肾脏的S - I放射性流出相似，但SHR肾脏的S - I升压反应增强。PGE2抑制且吲哚美辛增强WKY和SHR肾脏中放射性的S - I流出，程度相似。PGE2的这种抑制作用是由于抑制性节前PGE2受体的激活。神经元释放的去甲肾上腺素刺激局部PGE2的形成，然后通过跨突触抑制去甲肾上腺素释放。成年SHR中肾去甲肾上腺素释放及其受PGs的调节未改变。肾血管系统节后反应性增强可能有助于成年SHR高血压的维持。